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https://www.readbyqxmd.com/read/29163172/central-administration-of-5z-7-oxozeaenol-protects-experimental-autoimmune-encephalomyelitis-mice-by-inhibiting-microglia-activation
#1
Lingli Lu, Xiuping Zhang, Huichun Tong, Wenlong Zhang, Pingyi Xu, Shaogang Qu
Transforming growth factor β-activated kinase 1 (TAK1), a vital upstream integrator of multiple pro-inflammatory signaling pathways, mediates the production of pro-inflammatory cytokines, chemokines, and adhesion molecules. Investigations targeting TAK1 provide new therapeutic options for chronic inflammatory disorders, autoimmune diseases, and cancer. However, the role and mechanism of the TAK1 inhibitor 5Z-7-oxozeaenol in treating autoimmune demyelinating diseases remain unclear. This work aimed to identify whether 5Z-7-oxozeaenol exerts neuroprotective effects on experimental autoimmune encephalomyelitis (EAE) in mice...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29154963/macrophage-scavenger-receptor-1-contributes-to-pathogenesis-of-fulminant-hepatitis-via-neutrophil-mediated-complement-activation
#2
Yuan Tang, Huifang Li, Junru Li, Yunzhi Liu, Yanli Li, Jing Zhou, Jia Zhou, Xiao Lu, Wei Zhao, Jinlin Hou, Xiang-Yang Wang, Zhengliang Chen, Daming Zuo
BACKGROUND & AIMS: The macrophage scavenger receptor 1 (Msr1, also called SRA)is a pattern recognition receptor primarily expressed on myeloid cells, playing an important role in the maintenance of immune homeostasis. Since MSR1 expression was up-regulated in the livers of patients with fulminant hepatitis (FH), we investigated the functional mechanism of Msr1 as related to FH pathogenesis. METHODS: Msr1-deficient (Msr1(-/-)) mice and their wild-type (WT) littermates were infected with mouse hepatitis virus strain-A59 (MHV-A59) to induce FH, and the levels of tissue damage, serum alanine aminotransferase (ALT), inflammatory cytokines and complement C5a were measured and compared...
November 14, 2017: Journal of Hepatology
https://www.readbyqxmd.com/read/29150630/inhibition-of-myeloid-differentiation-primary-response-protein-88-provides-neuroprotection-in-early-brain-injury-following-experimental-subarachnoid-hemorrhage
#3
Huiying Yan, Dingding Zhang, Yongxiang Wei, Hongbin Ni, Weibang Liang, Huasheng Zhang, Shuangying Hao, Wei Jin, Kuanyu Li, Chun-Hua Hang
Accumulating of evidence suggests that activation of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) exacerbates early brain injury (EBI) following subarachnoid hemorrhage (SAH) by provoking pro-inflammatory and pro-apoptotic signaling. Myeloid differentiation primary response protein 88 (MyD88) is an endogenous adaptor protein in the toll-like receptors (TLRs) and interleukin (IL) -1β family signaling pathways and acts as a bottle neck in the NF-κB and MAPK pathways. Here, we used ST2825, a selective inhibitor of MyD88, to clarify whether inhibiting MyD88 could provide neuroprotection in EBI following SAH...
November 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29147012/piperidylmethyloxychalcone-improves-immune-mediated-acute-liver-failure-via-inhibiting-tak1-activity
#4
Sun Hong Park, Jeong-Ah Kwak, Sang-Hun Jung, Byeongwoo Ahn, Won-Jea Cho, Cheong-Yong Yun, Chang Seon Na, Bang Yeon Hwang, Jin Tae Hong, Sang-Bae Han, Youngsoo Kim
Mice deficient in the toll-like receptor (TLR) or the myeloid differentiation factor 88 (MyD88) are resistant to acute liver failure (ALF) with sudden death of hepatocytes. Chalcone derivatives from medicinal plants protect from hepatic damages including ALF, but their mechanisms remain to be clarified. Here, we focused on molecular basis of piperidylmethyloxychalcone (PMOC) in the treatment of TLR/MyD88-associated ALF. C57BL/6J mice were sensitized with D-galactosamine (GalN) and challenged with Escherichia coli lipopolysaccharide (LPS, TLR4 agonist) or oligodeoxynucleotide containing unmethylated CpG motif (CpG ODN, TLR9 agonist) for induction of ALF...
November 17, 2017: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/29145973/tak-ing-aim-at-chemoresistance-the-emerging-role-of-map3k7-as-a-target-for-cancer-therapy
#5
Raffaela Santoro, Carmine Carbone, Geny Piro, Paul J Chiao, Davide Melisi
Cellular drug resistance remains the main obstacle to the clinical efficacy of cancer chemotherapy. Alterations in key pathways regulating cell cycle checkpoints, apoptosis and Epithelial to Mesenchymal Transition (EMT), such as the Mitogen-activated protein kinase (MAPK) pathway, appear to be closely associated to cancer chemoresistance. Transforming growth factor-β (TGF-β)- activated kinase 1 (TAK1, also known as MAP3K7) is a serine/threonine kinase in the mitogen-activated protein kinase (MAP3K) family...
November 2017: Drug Resistance Updates: Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy
https://www.readbyqxmd.com/read/29143862/a20-prevents-obesity-induced-development-of-cardiac-dysfunction
#6
Wenjing Xu, Cheng Wang, Minglu Liang, Long Chen, Qin Fu, Fengxiao Zhang, Yan Wang, Dan Huang, Kai Huang
Obesity and an increased free fatty acid (FFA) level are tightly linked, leading to aberrant oxidative stress, inflammation, apoptosis, and progression to cardiovascular disorders. A20 is a ubiquitin-modifying enzyme that plays a significant role in the negative regulation of inflammatory response. Here, we study the role of A20 in obesity-induced heart injury and explore the underlying mechanisms. A20 expression was first increased in mouse hearts after 4 weeks of a high-fat diet (HFD) and then was gradually decreased in the following 20 weeks...
November 16, 2017: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/29138854/ng25-an-inhibitor-of-transforming-growth-factor%C3%A2-%C3%AE-%C3%A2-activated-kinase-1-ameliorates-neuronal-apoptosis-in-neonatal-hypoxic%C3%A2-ischemic-rats
#7
Hua Wang, Zhong Chen, Yu Li, Qiaoyun Ji
Transforming growth factor (TGF)‑β‑activated kinase 1 (TAK1) was found to be activated by TGF‑β and acts as a central regulator of cell death in various types of disease. However, the expression and function of TAK1 in the neonatal brain following hypoxia‑ischemia (HI) remains unclear. In the present study, western blotting and immunofluorescence were employed to determine the expression and distribution of TAK1 in the brain cortex of a perinatal HI rat model. In addition, the specific inhibitor of TAK1, NG25 was administered via intracerebroventricular injection, prior to insult of the neonatal rat brains, for neuroprotection...
November 10, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29128906/toll-like-receptor-3-mediates-hiv-1-induced-interleukin-6-expression-in-the-human-brain-endothelium-via-tak1-and-jnk-pathways-implications-for-viral-neuropathogenesis
#8
Biju Bhargavan, Georgette D Kanmogne
HIV-1-associated neurocognitive disorders (HAND) is associated with blood-brain-barrier (BBB) inflammation, and inflammation involves toll-like receptors (TLRs) signaling. It is not known whether primary human brain microvascular endothelial cells (HBMEC), the major BBB component, express TLRs or whether TLRs are involved in BBB dysfunction and HAND. We demonstrate that HBMEC express TLR3, 4, 5, 7, 9, and 10, and TLR3 was the most abundant. HIV-1 and TLR3 activation increased endothelial TLR3 transcription and expression...
November 11, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/29127073/estrogen-receptor-beta-maintains-expression-of-klf15-to-prevent-cardiac-myocyte-hypertrophy-in-female-rodents
#9
Neil Hoa, Lisheng Ge, Kenneth S Korach, Ellis R Levin
Maintaining a healthy, anti-hypertrophic state in the heart prevents progression to cardiac failure. In humans, angiotensin II (AngII) indirectly and directly stimulates hypertrophy and progression, while estrogens acting through estrogen receptor beta (ERβ) inhibit these AngII actions. The KLF15 transcription factor has been purported to provide anti-hypertrophic action. In cultured neonatal rat cardiomyocytes, we found AngII inhibited KLF1 expression and nuclear localization, substantially prevented by estradiol (E2) or β-LGND2 (β-LGND2), an ERβ agonist...
November 7, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/29119451/pristimerin-inhibits-lps-triggered-neurotoxicity-in-bv-2-microglia-cells-through-modulating-irak1-traf6-tak1-mediated-nf-%C3%AE%C2%BAb-and-ap-1-signaling-pathways-in-vitro
#10
Bin Hui, Liping Zhang, Qinhua Zhou, Ling Hui
Microglia plays a prominent role in the brain's inflammatory response to injury or infection by migrating to affected locations and secreting inflammatory molecules. However, hyperactivated microglial is neurotoxic and plays critical roles in the pathogenesis of neurodegenerative diseases. Pristimerin, a naturally occurring triterpenoid, possesses antitumor, antioxidant, and anti-inflammatory activities. However, the effect and the molecular mechanism of pristimerin against lipopolysaccharide (LPS)-induced neurotoxicity in microglia remain to be revealed...
November 8, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/29082699/-mechanism-in-growth-inhibition-of-quercetin-on-human-bladder-cancer-cell-line
#11
Da-Qing Tan, Xiao-Hua Liu
To investigate the inhibitory mechanism of quercetin on growth of human bladder cancer cell line(BIU-87). BIU-87 cells were cultured in vitro, and co-cultured with varying concentrations of quercetin, and the anti-proliferative activity was determined by CCK-8 assay. Apoptosis of quercetin-induced BIU-87 cells and cell cycle were determined by flow cytometry analysis. Expressions of Bal-2 and Bal-xL, and related proteins in TAK1/JNK signal pathway were measured using Western blot analysis. After treatment with quercetin for 24 h and 48 h, the proliferation of BIU-87 cells was significantly suppressed in a dose-dependent manner according to CCK-8 assay(P<0...
May 2017: Zhongguo Zhong Yao za Zhi, Zhongguo Zhongyao Zazhi, China Journal of Chinese Materia Medica
https://www.readbyqxmd.com/read/29077210/hepatocyte-dusp14-maintains-metabolic-homeostasis-and-suppresses-inflammation-in-the-liver
#12
Siyuan Wang, Zhen-Zhen Yan, Xia Yang, Shimin An, Kuo Zhang, Yu Qi, Jilin Zheng, Yan-Xiao Ji, Pi-Xiao Wang, Chun Fang, Xue-Yong Zhu, Li-Jun Shen, Feng-Juan Yan, Rong Bao, Song Tian, Zhi-Gang She, Yi-Da Tang
Non-alcoholic fatty liver disease (NAFLD) is a prevalent and complex disease that confers a high risk of severe liver disorders. Despite such public and clinical health importance, very few effective therapies are currently available for NAFLD. Herein, we reported a protective function and the underlying mechanism of dual-specificity phosphatase 14 (DUSP14) in NAFLD and related metabolic disorders. Insulin resistance, hepatic lipid accumulation and concomitant inflammatory responses, which are key pathological processes involved in NAFLD development, were significantly ameliorated by hepatocyte-specific DUSP14 overexpression (DUSP14-HTG) in high-fat diet (HFD)-induced or genetically obese mouse models...
October 27, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/29071539/knockdown-of-iars2-suppressed-growth-of-gastric-cancer-cells-by-regulating-the-phosphorylation-of-cell-cycle-related-proteins
#13
Zheng Fang, Xingyu Wang, Qiang Yan, Shangxin Zhang, Yongxiang Li
The purpose of the article is to investigate the role of IARS2 in proliferation, apoptosis, and cell cycle of gastric cancer (GC) cells in vitro. The IARS2-shRNA lentiviral vector was established and used to infect the GC cell line AGS. qRT-PCR and Western blot were employed to determine the efficiency of IARS2 knockdown. The effects of IARS2 knockdown on cell proliferation, cell clone formation, and cell cycle were assessed by MTT assay, colony formation assay, and flow cytometer analysis, respectively. Finally, a PathScan Antibody Array Kit was used to detect the expression levels of cell cycle-related proteins after IARS2 knockdown in AGS cells to elucidate the underlying mechanisms...
October 25, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/29059173/sox9-activity-is-induced-by-oncogenic-kras-to-affect-mdc1-and-mcms-expression-in-pancreatic-cancer
#14
H Zhou, Y Qin, S Ji, J Ling, J Fu, Z Zhuang, X Fan, L Song, X Yu, P J Chiao
SRY (sex determining region Y)-box 9 (SOX9) is required for oncogenic Kras-mediated acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neoplasias (PanINs) and ultimately pancreatic ductal adenocarcinoma (PDAC). However, how oncogenic Kras affects SOX9 activity is not yet understood, and SOX9-associated genes in PDAC are also unknown at all. Here, we investigated the mechanistic link between SOX9 and oncogenic Kras, studied biological function of SOX9, and identified SOX9-related genes and their clinical significance in patients with PDAC...
October 23, 2017: Oncogene
https://www.readbyqxmd.com/read/29038250/inhibition-of-irak1-ubiquitination-determines-glucocorticoid-sensitivity-for-tlr9-induced-inflammation-in-macrophages
#15
Fansheng Kong, Zhiwei Liu, Viral G Jain, Kenjiro Shima, Takuji Suzuki, Louis J Muglia, Daniel T Starczynowski, Chandrashekhar Pasare, Sandip Bhattacharyya
Inflammatory responses are controlled by signaling mediators that are regulated by various posttranslational modifications. Recently, transcription-independent functions for glucocorticoids (GC) in restraining inflammation have emerged, but the underlying mechanisms are unknown. In this study, we report that GC receptor (GR)-mediated actions of GC acutely suppress TLR9-induced inflammation via inhibition of IL-1R-associated kinase 1 (IRAK1) ubiquitination. β-TrCP-IRAK1 interaction is required for K48-linked ubiquitination of IRAK1 at Lys(134) and subsequent membrane-to-cytoplasm trafficking of IRAK1 interacting partners TNFR-associated factor 6 and TAK1 that facilitates NF-κB and MAPK activation...
November 15, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29029426/a20-functions-as-mediator-in-tnf%C3%AE-induced-injury-of-human-umbilical-vein-endothelial-cells-through-tak1-dependent-mapk-enos-pathway
#16
Lei Li, Bingqing Huang, Shiyang Song, Hareshwaree Sohun, Zhiheng Rao, Luyuan Tao, Qike Jin, Jingjing Zeng, Rongzhou Wu, Kangting Ji, Jiafeng Lin, Lianpin Wu, Maoping Chu
A20, a negative regulator of nuclear factor κB signaling, has been shown to attenuate atherosclerotic events. Transforming growth factor beta-activated kinase 1 (TAK1) plays a critical role in TNFα-induced atherosclerosis via endothelial nitric oxide (NO) synthase (eNOS) uncoupling and NO reduction. In the study, we investigated the hypothesis that A20 protected endothelial cell injury induced by TNFα through modulating eNOS activity and TAK1 signalling. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNFα...
September 12, 2017: Oncotarget
https://www.readbyqxmd.com/read/29027124/tak1-inhibition-ameliorates-survival-from-graft-versus-host-disease-in-an-allogeneic-murine-marrow-transplantation-model
#17
Ayako Kobayashi, Shinichi Kobayashi, Kosuke Miyai, Yukiko Osawa, Toshikatsu Horiuchi, Shoichiro Kato, Takaaki Maekawa, Takeshi Yamamura, Junichi Watanabe, Ken Sato, Hitoshi Tsuda, Fumihiko Kimura
Acute graft-versus-host disease (GVHD) is a major cause of morbidity and mortality in allogeneic hematopoietic cell transplantation (allo-HCT). Majority of the current immunosuppressive strategies targeting donor T cells to prevent or treat acute GVHD are only partially effective, and often require escalated immunosuppressive therapy. Recent studies have revealed that activation of antigen-presenting cells in the proinflammatory milieu is important for the priming and promotion of GVHD. This activation is mediated by innate immune signaling pathways, which therefore potentially represent new targets in addressing GVHD...
October 12, 2017: International Journal of Hematology
https://www.readbyqxmd.com/read/29024853/overexpression-of-constitutively-active-map3k7-in-ameloblasts-causes-enamel-defects-of-mouse-teeth
#18
Zhao Jinping, Chu Qing, Song Wenying, Yang Chunyan, Xiang Lili, Shi Yao, Wang Yumin, Xu Zhenzhen, Zhang Li, Gao Yuguang
OBJECTIVE: Compelling evidence suggests that mitogen-activated protein kinases (Mapks) play an important role in amelogenesis. However, the role of transforming growth factor (TGF)-β-activating kinase 1 (Tak1, Map3k7), which is a known upstream kinase of Mapks, during amelogenesis remains to be determined. The aim of this study was to investigate the possible involvement of Map3k7 in amelogenesis. DESIGN: We generated transgenic mice that produced constitutively active human MAP3K7 (caMAP3K7) under the control of amelogenin (Amelx) gene promoter...
September 25, 2017: Archives of Oral Biology
https://www.readbyqxmd.com/read/28993672/oligomerization-primed-coiled-coil-domain-interaction-with-ubc13-confers-processivity-to-traf6-ubiquitin-ligase-activity
#19
Lin Hu, Jiafeng Xu, Xiaomei Xie, Yiwen Zhou, Panfeng Tao, Haidong Li, Xu Han, Chong Wang, Jian Liu, Pinglong Xu, Dante Neculai, Zongping Xia
Ubiquitin ligase TRAF6, together with ubiquitin-conjugating enzyme Ubc13/Uev1, catalyzes processive assembly of unanchored K63-linked polyubiquitin chains for TAK1 activation in the IL-1R/TLR pathways. However, what domain and how it functions to enable TRAF6's processivity are largely uncharacterized. Here, we find TRAF6 coiled-coil (CC) domain is crucial to enable its processivity. The CC domain mediates TRAF6 oligomerization to ensure efficient long polyubiquitin chain assembly. Mutating or deleting the CC domain impairs TRAF6 oligomerization and processive polyubiquitin chain assembly...
October 9, 2017: Nature Communications
https://www.readbyqxmd.com/read/28989054/nuclear-met-promotes-hepatocellular-carcinoma-tumorigenesis-and-metastasis-by-upregulation-of-tak1-and-activation-of-nf-%C3%AE%C2%BAb-pathway
#20
Sze Keong Tey, Edith Yuk Ting Tse, Xiaowen Mao, Frankie Chi Fat Ko, Alice Sze Tsai Wong, Regina Cheuk-Lam Lo, Irene Oi-Lin Ng, Judy Wai Ping Yam
Presence of Met receptor tyrosine kinase in the nucleus of cells has been reported. However, the functions of Met which expresses in the nucleus (nMet) remain elusive. In this study, we found that nMet was increased in 89% of HCC tumorous tissues when compared with the corresponding non-tumorous liver tissues. nMet expression increased progressively along HCC development and significantly correlated with cirrhosis, poorer cellular differentiation, venous invasion, late stage HCC and poorer overall survival...
October 6, 2017: Cancer Letters
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